Theca Cell Function in Adolescents With Polycystic Ovary Syndrome (PCOS)
| Status: | Completed |
|---|---|
| Conditions: | Women's Studies |
| Therapuetic Areas: | Reproductive |
| Healthy: | No |
| Age Range: | 12 - 18 |
| Updated: | 4/21/2016 |
| Start Date: | August 2011 |
| End Date: | September 2014 |
In women with polycystic ovary syndrome (PCOS), the cardinal physiological abnormality is
excessive ovarian androgen production marked by increased serum testosterone (T) and
androstenedione (A) levels. Studies to determine the alteration in ovarian steroidogenesis
that lead to abnormal production of ovarian androgens have revealed increased CYP17 gene
expression with accentuated 17-hydroxylase activity leading to exaggerated
17-hydroxyprogesterone (17P) responses to luteinizing hormone (LH) stimulation. In contrast,
T and A responses did not distinguish between PCOS and normal women, although these
androgens were clearly greater in the former compared to the latter group. As a result, 17P
responsiveness has been employed to determine the functional capacity of the ovary to
produce androgens. The stimulatory agents that have been used included GnRH agonist, Lupron,
at a dose of 10 microgram per kilogram, or hCG at a dose of 10,000 IU. The investigators
propose to conduct a study that will determine the pattern of androgen responsiveness to
25ucg of hCG after 24 hours in adolescents with PCOS, those with oligomenorrhea, and in
normal controls. This will allow for a comparison of these adolescents' ovarian functional
capacity to produce androgens.
excessive ovarian androgen production marked by increased serum testosterone (T) and
androstenedione (A) levels. Studies to determine the alteration in ovarian steroidogenesis
that lead to abnormal production of ovarian androgens have revealed increased CYP17 gene
expression with accentuated 17-hydroxylase activity leading to exaggerated
17-hydroxyprogesterone (17P) responses to luteinizing hormone (LH) stimulation. In contrast,
T and A responses did not distinguish between PCOS and normal women, although these
androgens were clearly greater in the former compared to the latter group. As a result, 17P
responsiveness has been employed to determine the functional capacity of the ovary to
produce androgens. The stimulatory agents that have been used included GnRH agonist, Lupron,
at a dose of 10 microgram per kilogram, or hCG at a dose of 10,000 IU. The investigators
propose to conduct a study that will determine the pattern of androgen responsiveness to
25ucg of hCG after 24 hours in adolescents with PCOS, those with oligomenorrhea, and in
normal controls. This will allow for a comparison of these adolescents' ovarian functional
capacity to produce androgens.
In women with polycystic ovary syndrome (PCOS), the cardinal physiological abnormality is
excessive ovarian androgen production marked by increased serum testosterone (T) and
androstenedione (A) levels. Studies to determine the alteration in ovarian steroidogenesis
that lead to abnormal production of ovarian androgens have revealed increased CYP17 gene
expression with accentuated 17-hydroxylase activity leading to exaggerated
17-hydroxyprogesterone (17P) responses to luteinizing hormone (LH) stimulation. In contrast,
T and A responses did not distinguish between PCOS and normal women, although these
androgens were clearly greater in the former compared to the latter group. As a result, 17P
responsiveness has been employed to determine the functional capacity of the ovary to
produce androgens. The stimulatory agents that have been used included GnRH agonist, Lupron,
at a dose of 10 microgram per kilogram, or hCG at a dose of 10,000 IU.We propose to conduct
a study that will determine the pattern of androgen responsiveness to 25ucg of hCG after 24
hours in adolescents with PCOS, those with oligomenorrhea, and in normal controls. This will
allow for a comparison of these adolescents' ovarian functional capacity to produce
androgens.
excessive ovarian androgen production marked by increased serum testosterone (T) and
androstenedione (A) levels. Studies to determine the alteration in ovarian steroidogenesis
that lead to abnormal production of ovarian androgens have revealed increased CYP17 gene
expression with accentuated 17-hydroxylase activity leading to exaggerated
17-hydroxyprogesterone (17P) responses to luteinizing hormone (LH) stimulation. In contrast,
T and A responses did not distinguish between PCOS and normal women, although these
androgens were clearly greater in the former compared to the latter group. As a result, 17P
responsiveness has been employed to determine the functional capacity of the ovary to
produce androgens. The stimulatory agents that have been used included GnRH agonist, Lupron,
at a dose of 10 microgram per kilogram, or hCG at a dose of 10,000 IU.We propose to conduct
a study that will determine the pattern of androgen responsiveness to 25ucg of hCG after 24
hours in adolescents with PCOS, those with oligomenorrhea, and in normal controls. This will
allow for a comparison of these adolescents' ovarian functional capacity to produce
androgens.
Inclusion Criteria:
- Normal CBC (Hemoglobin must be at least 11mg/dl)
- Normal renal and liver function tests
- Normal vital signs including normal blood pressure
Exclusion Criteria:
- Pregnancy
- On oral contraceptives
- On insulin lowering drugs
- On anti-androgens (i.e., spironolactone, flutamide, finasteride, etc)
- On medications that will influence androgen metabolism or clearance
- On medications that will inhibit the cytochrome P450 enzyme system (Cimetidine,
ketoconazole, etc)
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